Bob
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Association of mitochondrial dysfunction and fatigue: A review of the literature.
Kristin Filler, Debra Lyon, James Bennett, Nancy McCain, Ronald Elswick, Nada Lukkahatai, Leorey N. Saligan.
BBA Clinical, Available online 13 April 2014
http://www.sciencedirect.com/science/article/pii/S221464741400004X
This is very much a CFS-related paper: The study reviewed 25 papers, 18 of which investigated only patients with chronic fatigue syndrome (CFS), with three more investigating ME, or ME and CFS:
"Eighteen studies investigated only patients with chronic fatigue syndrome (CFS); remaining studies investigated a combination of myalgic encephalomyelitis (ME) and CFS (n = 2), ME (n = 1), multiple sclerosis (n = 1), HIV-related fatigue (HRF) (n = 1), systemic lupus erythematosus (SLE) (n = 1), and cancer-related fatigue (CRF) (n = 1)."
Kristin Filler, Debra Lyon, James Bennett, Nancy McCain, Ronald Elswick, Nada Lukkahatai, Leorey N. Saligan.
BBA Clinical, Available online 13 April 2014
http://www.sciencedirect.com/science/article/pii/S221464741400004X
This is very much a CFS-related paper: The study reviewed 25 papers, 18 of which investigated only patients with chronic fatigue syndrome (CFS), with three more investigating ME, or ME and CFS:
"Eighteen studies investigated only patients with chronic fatigue syndrome (CFS); remaining studies investigated a combination of myalgic encephalomyelitis (ME) and CFS (n = 2), ME (n = 1), multiple sclerosis (n = 1), HIV-related fatigue (HRF) (n = 1), systemic lupus erythematosus (SLE) (n = 1), and cancer-related fatigue (CRF) (n = 1)."
Abstract
Fatigue is often described by patients as a lack of energy, mental or physical tiredness, diminished endurance, and prolonged recovery after physical activity. Etiologic mechanisms underlying fatigue are not well understood; however, fatigue is a hallmark symptom of mitochondrial disease, making mitochondrial dysfunction a putative biological mechanism for fatigue. Therefore, this review examined studies that investigated the association of markers of mitochondrial dysfunction with fatigue and proposes possible research directions to enhance understanding of the role of mitochondrial dysfunction in fatigue. A thorough search using PubMed, Scopus, Web of Science, and Embase databases returned 1220 articles. After the application of inclusion and exclusion criteria, a total of 25 articles meeting eligibility criteria were selected for full review. Dysfunctions in the mitochondrial structure, mitochondrial function (mitochondrial enzymes and oxidative/nitrosative stress), mitochondrial energy metabolism (ATP production and fatty acid metabolism), immune response, and genetics were investigated as potential contributors to fatigue. Carnitine was the most investigated mitochondrial function marker. Dysfunctional levels were reported in all the studies investigating carnitine; however, the specific type of carnitine that was dysfunctional varied. Genetic profiles were the second most studied mitochondrial parameter. Six common pathways were proposed: metabolism, energy production, protein transport, mitochondrial morphology, central nervous system dysfunction and post-viral infection. Coenzyme Q10 was the most commonly investigated mitochondrial enzyme. Low levels of Coenzyme Q10 were consistently associated with fatigue. Potential targets for further investigation were identified as well as gaps in the current literature.